Abstract
BackgroundDespite marked advances in our understanding of the pathophysiology of the coronary slow flow phenomenon (CSFP), the exact mechanism remains unclear. Previous studies have suggested that CSFP might be associated with generalized atherosclerosis, endothelial dysfunction, and low-grade chronic inflammation. High serum alkaline phosphatase (ALP) levels are associated with vascular calcification, atherosclerotic disease, and an increased risk of cardiovascular events. However, the relationship between ALP and CSFP is unclear.MethodsWe investigated 64 patients with angiographically proven CSFP and 50 with normal coronary flow. Serum ALP levels were measured in all studied individuals.ResultsSerum ALP levels in patients with CSFP were significantly higher than those in the control group (70.5 ± 17.1 vs. 61.9 ± 16.1 U/L, P = 0.007). A positive association was observed (r = 0.42, P = 0.032) between serum ALP levels and the mean thrombolysis in myocardial infarction frame count (mTFC). Regression analysis showed a high serum ALP level was the only independent predictor of the mTFC (β = 0.309, P < 0.001). Moreover, our study showed that a serum ALP level > 67.5 U/L was a predictor of CSFP (sensitivity = 83.3%, specificity = 84.1%).ConclusionsPatients with CSFP show high serum ALP levels, which may be associated with the pathogenesis of CSFP. A high serum ALP level is a predictor of CSFP. Future studies are needed to clarify the role of ALP in patients with CSFP.
Highlights
Despite marked advances in our understanding of the pathophysiology of the coronary slow flow phenomenon (CSFP), the exact mechanism remains unclear
[7] and endothelial dysfunction [8], which have been reported in several studies, along with chronic inflammation [8,9,10,11] and diffuse atherosclerosis are [12] considered underlying etiologies associated with CSFP; the exact etiology of CSFP remains unclear
This study showed that the serum alkaline phosphatase (ALP) level was significantly elevated in patients with CSFP and moderately associated with the myocardial infarction frame count (mTFC)
Summary
Despite marked advances in our understanding of the pathophysiology of the coronary slow flow phenomenon (CSFP), the exact mechanism remains unclear. The coronary slow flow phenomenon (CSFP) is characterized by normal or near-normal epicardial coronary arteries (stenosis < 40%) but delayed distal vessel opacification using a contrast agent during diagnostic coronary angiography [1] This angiographic entity was first discovered by Tambe et al in 1972 [2]. Microvascular [7] and endothelial dysfunction [8], which have been reported in several studies, along with chronic inflammation [8,9,10,11] and diffuse atherosclerosis are [12] considered underlying etiologies associated with CSFP; the exact etiology of CSFP remains unclear. Because the pathogenesis of CSFP and the role of ALP is similar, we investigated the relationship between the 2 and attempted to suggest new insights into the development of CSFP
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